Rickets and osteomalacia not associated with steatorrhea, renal tubular acidosis, or the Fanconi syndrome, yet resistant to treatment with vitamin D, continue to be a perplexing medical problem. Whether the condition represents a true resistance to the action of vitamin D or a primary renal tubular defect for phosphorus reabsorption has not as yet been resolved. Treatment has consisted of large doses of oral vitamin D, and while radiologic improvement may be apparent after such therapy, the striking hypophosphatemia of the disorder is often unaffected, and undesirable hypercalcemia may occur.
Two of us 1,2 have previously reported on the efficacy of oral phosphate supplements in two adult patients with acquired osteomalacia of the vitamin-D-refractory type (phosphate diabetes). Both patients had severe bone pain, pseudofractures, hypophosphatemia, increased levels of serum alkaline phosphatase, and widened osteoid seams in bone obtained by biopsy. The usual causes of osteomalacia such as malnutrition, steatorrhea, and